Abstract
In area CA1 of the hippocampus, long-term depression (LTD) can be induced by activating group I metabotropic glutamate receptors (mGluRs), with the selective agonist DHPG. There is evidence that mGluR-LTD can be expressed by either a decrease in the probability of neurotransmitter release [P(r)] or by a change in postsynaptic AMPA receptor number. However, what determines the locus of expression is unknown. We investigated the expression mechanisms of mGluR-LTD using either a low (30 μM) or a high (100 μM) concentration of (RS)-DHPG. We found that 30 μM DHPG generated presynaptic LTD that required the co-activation of NMDA receptors, whereas 100 μM DHPG resulted in postsynaptic LTD that was independent of the activation of NMDA receptors. We found that both forms of LTD occur at the same synapses and that these may constitute the population with the lowest basal P(r). Our results reveal an unexpected complexity to mGluR-mediated synaptic plasticity in the hippocampus.
| Original language | English |
|---|---|
| Article number | 857675 |
| Journal | Frontiers in Synaptic Neuroscience |
| Volume | 14 |
| DOIs | |
| Publication status | Published - 9 May 2022 |
Bibliographical note
Funding Information:This study was supported by the World-Class University Program, the Creative Research Initiative Program of the Ministry of Science and Technology in Korea, and the National Honor Scientist Program of the National Research Foundation funded by the Korea Government (B-KK), the Medical Research Council, United Kingdom (GC), and the Biotechnology and Biological Science Research Council (GC). GC was also supported by the Krembil Family Chair in Alzheimer’s Research and the Canadian Institute of Health Research.
Publisher Copyright:
Copyright © 2022 Sanderson, Ralph, Amici, Ng, Kaang, Zhuo, Kim, Georgiou and Collingridge.